There has been much effort recently to explore the role of adipocytokines in the interaction between adipose tissue, inflammation, and immunity. Tumor necrosis factor-alpha, interleukin-6, resistin, and many other adipocytokines are the soluble mediators derived mainly from adipocytes (fat cells). They are known to influence insulin sensitivity and glucose metabolism profoundly, thus providing a molecular link between increased adiposity and insulin resistance (IR). Resistin, an adipocytokine, is a member of a class of cysteine-rich proteins, collectively termed resistin-like molecules. They were initially discovered in rodents. It is present in gross visceral fat deposits and is released by adipocytes in humans. Owing to the regional variation in the expression of resistin mRNA and protein levels in humans, the highest levels have been noted in the abdominal depot. It is interesting to note that resistin also gets released from infiltrating white blood cells subsequent to subclinical chronic low-grade inflammatory response, accompanying obesity. This convergence of adipocyte and macrophage function in obese Type II diabetics has paved its role in molecular linkage of obesity, inflammation and metabolic syndrome (MetS) risk. Resistin, being a pro-inflammatory adiopokine, contributes to atherosclerosis. High serum resistin levels have been found, although with some inconsistencies, in cardiovascular patients, labeling it as a cardiovascular disease (CVD) marker, to predict incident cardiovascular events. Both IR and inflammation are the pathogenic factors contributing to increased risk of CVD, associated with diabetes, thus tagging resistin as a potential MetS marker. In conclusion, resistin is a fascinating new hormone awaiting further research in the obesity – IR – diabetes – MetS link.

Autoimmune Polyglandular Syndrome (APS) is characterized by presence of immune dysfunction of two or more endocrine glands and other non-endocrine organs. Only few cases of APS III associated with different immunological or genetic disorders have been reported. We present a 17-year old boy presented with easy fatigability, recurrent abdominal pain, pallor and language impairment; evaluated to have Autoimmune Thyroiditis, Megaloblastic Anemia due to vitamin B12 deficiency and Type 1 Diabetes Mellitus; with final diagnosis as APS IIIB with Immune Thrombocytopenia, leucopenia and Beta Thalessemia trait. The child requires lifelong monitoring of glandular functions and hormone replacement therapy for established glandular failure or failures. APS IIIB is as yet known to occur in middle aged women. It should be suspected in younger ages and diagnosed early to prevent the complications associated with the chronic endocrine deficiencies.

Hypothyroidism can present with a wide range of nonspecific symptoms, some of which are cutaneous. However, hypothyroidism presenting as isolated palmar hyperkeratosis is rarely described in the literature. Here, we describe a 30-year-old male who presented with hyperkeratosis and painful fissures of both palms for 1½ years' duration. He had minimal relief with keratolytic agents. On physical examination, he was found to have bradycardia and when investigated he was found to have severe hypothyroidism. A diagnosis of autoimmune hypothyroidism was made after further laboratory studies. He was treated with thyroxine, and a gradual improvement of hyperkeratosis was noted over a period of 3 months. Although extremely rare, clinicians should consider hypothyroidism as a cause of hyperkeratosis, especially when it is refractory to treatment and/or there are other possible symptoms of hypothyroidism.